From 11/1995 to 4/1999 we treated by prednisone for 15 patients and CsA for 16 ones with idiopathic aplastic anemia. Results:- Prednison did not change significantly TCD3, TCD4 and TCD8 colony count comparing with pre-treatment (P>0.05).- CsA decreased clearly TCD3 colony count after 1st, 6th month (P<0,05). However, TCD4 colony count decreased not significantly (P>0.05). Conclusions: CsA has more suppressive effect on T-cell colonies, mainly TCDz3 and TCD8 than Prednisone and therefore it may be chosen to treat patients with idiopathic aplastic anemia without indication for bone marrow transplantation.
Anemia, Aplastic ; therapy ; blood ; therapeutics ; cyclosporine

Background: Patients who received multiple transfusions of blood and blood products may produce antibodies against antigens of erythrocytes, leukocytes, platelets etc, resulting in many clinical implications. Objectives: To detect frequencies of antineutrophil antibodies in multitransfused patients at National Institute of Hematology and Blood Transfusion (NIHBT). Subjects and methods: The study was conducted on 30 multitransfused patients. Among them there were 12 with thrombocytopenia and 18 with aplastic anemia. Results: 6 cases had anti - neutrophil antibodies, of which 5 had more than 5 times of transfusion, 4 with aplastic anemia and 2 with thrombocytopenia. The sera were further tested with neutrophil panel, revealing 4 samples with anti - NA 1 (13.3%) and 1 sample with anti - NA2 (3.3%). The frequency of anti - neutrophil antibodies in multitransfused patients at IHBT in the study is 20%. Conclusion: Frequency of anti-NA1 was higher than anti-NA2 in multitransfused patients at NIHBT and directly proportional by frequency of NA1 and NA2 antigens in this group. The technical process to identify and classify antineutrophil antibodies in this study can be applied for patients who received multiple transfusions of blood and blood products in Viet Nam
Anemia ; Aplastic/ blood ; complications ; pathology ; Neutrophils

Anemia, Aplastic ; therapy ; Fetal Blood ; transplantation ; Humans ; Mesenchymal Stromal Cells

OBJECTIVES: To quantitate apoptosis and Fas antigen expression of T lymphocytes by activation in aplastic anemia (AA) and compare with that of normal controls and completely-recovered AA, and to investigate the apoptotic sensitivity to anti-fas antibody of activated T lymphocytes in AA. METHODS: We studied the expression of Fas antigen on fresh T lymphocytes of twenty patients with AA [13 newly diagnosed, 7 recorvered AA after immunosuppressive therapy (IST)], and investigated the activation-induced cell death (AICD) and Fas expression by activation [interleukin-2 (200 U/ml) and phytohemagglutinin (50 micrograms/ml)] in 5 newly-diagnosed AA, 5 normal controls and 5 AA in complete response (CR). Apoptotic sensitivity to anti-Fas antibody was assessed by the time-course kinetics of induction of cell death by anti-Fas antibody (500 ng/ml). RESULTS: There was no significant difference of Fas antigen expression on freshly-isolated T lymphocytes among newly-diagnosed severe AA, normal control s and patients with AA in CR after IST. In normal controls, T lymphocytes death was greatly increased at 3 days of activation, and Fas antigen expression on T lymphocytes was increased above baseline at day 1 of activation. In contrast, in newly-diagnosed AA, T lymphocytes showed delayed cell death, which correlated with a slowed increase of Fas antigen expression by activation. Also, anti-Fa s antibody sensitivity of activated T lymphocytes was decreased in newly-diagnosed AA. In completely recovered AA, these abnormal AICD and Fas antigen expressions by activation were recovered to normal range. CONCLUSIONS: Abnormal AICD plays a role in the immune pathophysiology of AA, and defective Fas system is involved in this process.
Anemia, Aplastic/pathology ; Anemia, Aplastic/immunology* ; Antigens, CD95/blood ; Apoptosis ; Case-Control Studies ; Human ; In Vitro ; Lymphocyte Transformation ; T-Lymphocytes/pathology* ; T-Lymphocytes/immunology* ; Time Factors

Aplastic anemia is a rare complication of pregnancy that is associated with significant maternal and fetal morbidity and mortality. The relationship between aplastic anemia and pregnancy is not yet clear. Aplastic anemia in pregnancy is difficult to manage because the risk of bleeding and infection is high, especially in refractory to platelet transfusion. There is no therapeutic guide-line and prognosis for aplastic anemia in pregnancy refractory to platelet transfusion. We recently experienced one case of aplastic anemia in pregnancy refractory to platelet transfusion without no peripartum complication. So we report this case with brief review of the literature.
Anemia, Aplastic* ; Blood Platelets* ; Hemorrhage ; Mortality ; Peripartum Period ; Platelet Transfusion* ; Pregnancy* ; Prognosis

OBJECTIVETo evaluate bone marrow hematopoietic cells genetic instability (BMHCGI) in patients with aplastic anemia (AA) and to explore its influence on immunosupressive therapy for AA and significance on late clonal hematologic disorders.

METHODSGenetic instability of bone marrow mononuclear cells (BMMNC) was measured by Comet assay. The relationship between bone marrow failure parameters and genetic instability results was evaluated. The reciprocity of genetic instability and treatment responses to immunosuppressive therapy (IST) was investigated.

RESULTSComet assay parameters \[tail moment (TM), olive TM (OTM), comet %\] of AA patients were significantly higher than that of control group (P < 0.05). There was no statistic correlation of comet parameters of severe AA (SAA) BM hematopoietic cells with age, gender and peripheral blood cell count (P > 0.05). For the treatment response rate at six months after IST there was no statistical difference between comet cells of < 21.64% and of >/= 21.64%, and so did between OTM < 1.58 and >/= 1.58 in SAA patients. IST had no effect on SAA BMHCGI, whereas, the Comet%, TM and OTM in SAA PR patients and Comet% in CR patients were significantly decreased than those before treatment. Comet parameters of two SAA patients were significantly increased before the development of clonal cytogenetic abnormalities.

CONCLUSIONSIncreased BMHCGI may be one of the elements in the pathogenetic mechanisms in AA. The genetic instability is irrelevant to the SAA patients overall response rate of IST at six months, but IST can alleviate the genetic instabilities in responded SAA patients.

OBJECTIVETo evaluate the impact of recombinant human thrombopoietin (rhTPO) on short-term response of immunosuppressive therapy (IST) in patients with newly diagnosed acquired severe aplastic anemia (SAA).

METHODSThe clinical data of forty adult acquired SAA patients, who treated with IST combined with rhTPO, were retrospective analyzed and the hematologic recovery were compared with patients by the IST alone during the same period. The factors affecting the short-term response were also analyzed.

RESULTSAt 3 months after IST, both the total response rate and CR+GPR rate in rhTPO group were much higher than those in control group (75.0% vs 50.0%, P=0.022; and 17.5% vs 2.5%, P=0.025). At 6 months after IST, there was no difference of total hematologic response rate in rhTPO group and control group (77.5% vs 57.5%, P=0.058), while the CR+GPR rate was still higher in rhTPO group (45.0% vs 22.5%, P=0.033). The median time of platelet transfusion independence was much shorter in rhTPO group [33(0-90) vs 53(0-75) d, P=0.019]. Patients in rhTPO group needed less platelets transfusion support. The median platelet count in rhTPO group was 29(4-95)×10⁹/L at 3 months after IST, which was much higher than that in control group [29(4-95)×10⁹/L, P=0.006]. There was no significant difference regarding overall survival between the two groups (100.0% vs 91.0%, P=0.276).

CONCLUSIONrhTPO is effective in promoting platelet recovery and improving the hematopoietic response for SAA patients with IST.

Aplastic anemia is a hematopoietic disorder characterized by marked reduction or absence of erythoid, granulocytic, and megakariocytic cells in the bone marrow with resultant pancytopenia. To control of infection & bleeding secondary to leukopenia and thrombocytopenia, the inflammatory lesions in oral & maxillofacial area should be removed. MATERIALS AND METHOD: The extractions were performed on 21 patients with severe aplastic anemia. The initial, pre-operative and postoperative CBCs were checked up. Amount and kind of transfused platelet in each patient and increment of platelet level were recorded. The complications were documented. RESULT: A mean of 2.9 teeth were extracted from each patient(ranging between 1 and 13). Furthermore, surgical extractions including ostectomy and odontectomy of the third molar were performed on 11 patients. The preoperative WBC levels presented between 600/muL and 5000/muL(mean 2376/muL). The WBC values decreased by an average of 145/muL per patient after extractions had been performed. The teeth of 16 patients were extracted under 10.0g/dL, and the mean change in postoperative hemoglobin levels in comparison with preoperative hemoglobin levels was -0.06 per patient. The initial platelet levels were between 1000/(L and 81,000/muL(mean 20,174/muL). In five patients, extractions were performed with platelet levels less than 50,000/muL. CONCLUSION: The results suggest that more active and preventive treatments in the oral and maxillofacial area are possible and are necessary to remove the infectious foci on the patients with severe aplastic anemia. We report the results of our experiences and literature reviews in treatment of the patients with severe aplastic anemia in our department.
Anemia, Aplastic* ; Blood Platelets ; Bone Marrow ; Hemorrhage ; Humans ; Leukopenia ; Molar, Third ; Pancytopenia ; Surgery, Oral* ; Thrombocytopenia ; Tooth

Aplastic anemia is characterized by a failure of blood cell production resulting in varying degrees of pancytopenia with a markedly hypocellular bone marrow. Most cases of aplastic anemia are acquired, but the disease may also occur as the result of inherited abnormalities. In 50-65% of cases, however, the etiology is unknown. For acquired forms of aplastic anemia, a variety of causative factors, including radiation, viruses, chemicals and drugs, have been implicated. Antithyroid drugs(Carbimazole, Methimazole, Propylthiouracil) are usually listed among agents associated with the development of agranulocytosis, but aplastic anemia rarely follows their use. The first case of aplastic anemia followmg propylthiouracil was reported by Marte~lo et al. in 1967 and the second case was by Aksoy and Erdem in 1968. Recently, we experienced two cases of aplastic anemia following propylthiouracil therapy due to Graves disease, so we report here these cases with literature review.
Agranulocytosis ; Anemia, Aplastic* ; Blood Cells ; Bone Marrow ; Graves Disease ; Methimazole ; Pancytopenia ; Propylthiouracil*

Aplastic anemia is a serious hematological disorder characterized by pancytopenia and bone marrow hypocellularity. Pregnancy associated with aplastic anemia is fortunately uncommon considering the significant morbidity and mortality for both mother and the fetus. The risk to the mother is mainly in the form of hemorrhage and sepsis, while the fetus may suffer from growth restriction and even intrauterine death. Maternal mortality has been reported variously from 20% to 60%. The relationship between pregnancy and aplastic anemia remains controversial. We experienced a patient with severe aplastic anemia in pregnancy who was treated with supportive transfusion of red blood cells and platelets. Here, we present a case with a brief review of the literature.
Anemia, Aplastic ; Blood Platelets ; Bone Marrow ; Erythrocytes ; Fetus ; Hemorrhage ; Humans ; Maternal Mortality ; Mothers ; Pancytopenia ; Pregnancy ; Sepsis